Why is my calcium too high?

Ken: This 78 year old presented for evaluation of hypercalcemia. She was incidentally found to have a serum calcium of 10.9 mg/dl. At that time her PTH was 75, phosphate was 2.8 and 25-OH vitamin D was 17 ng/dl. Patient was on HCTZ which was discontinued. 6 weeks later a repeat serum calcium was 11.1 mg/dl and remained high at 11.3 mg/dl on repeat. The third serum calcium was drawn without a tourniquet. Her serum ionized calcium was also elevated. A urine calcium was 45 mg/24 hr.

Ken: Is this simple hyperparathyroidism or does the urine calcium worry you?

Steve: While there is no 24hr creatinine value for the 24hr urine collection, the low amount of calcium is surprising. Her elevated PTH suggests PTH mediated hypercalcemia, but primary hyperparathyroidism is not the only cause of primary hyperparathyroidism. The other important consideration is FHH or familial hypercalciuric hypocalcemia. Rather than a disorder of PTH secretion, FHH is an autosomal dominant mutation of the calcium sensing receptor itself. This essentially changes the calcium setpoint in the body, causing the body to adjust to a higher calcium level than the general population. The kidney has both PTH receptors as well as calcium sensing receptors (Goltzman, endotext.org). In the setting of primary hyperparathyroidism, since the calcium sensing receptor is functioning normally, the kidney should appropriately try to clear the elevated calcium. This leads to high urinary calcium. Over time this increases risk of volume depletion, kidney stones and nephrocalcinosis. Conversely in FHH, since the calcium receptor both for PTH secretion and at the level of the kidney has been altered, the calcium is very low in the urine as the kidney treats the serum calcium as a normal value. FHH is felt to be a benign condition so no intervention is necessary. In that case a surgical “correction” could carry risk of harm with no real benefit.

While the patient’s kidney function is not commented on and her phosphorus level is normal, as kidney function worsens the kidney loses the ability to secrete calcium which can mimic the low calcium level. This can make diagnosing primary hyperparathyroidism in the setting of renal disease quite complex.

Ken: FHH certainly is a consideration in this case. However, given her age of 78 and that she has siblings it seems unlikely none would have been diagnosed with hypercalcemia. I asked her to contact her two living sisters to see if they had diagnosed with hypercalcemia. Both her sisters denied this. One sister actually went to her doctor to be evaluated for elevated calcium after her sister had complained, and this sister’s levels were normal. FHH seems unlikely in this scenario. I believe that she has primary hyperparathyroidism and that her low urine calcium is due to both PTH’s resorption effect on tubules and her abnormal renal function is unable to compensate.

Goltzman, David. Approach to Hypercalcemia. Endotext.org. updated October 26 2019, accessed May 2022.

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